C. Miret et al., Relationship of oncogenes (sFas, bcl-2) and cytokines (IL-10, alfa-TNF) with the activity of systemic lupus erythematosus, ANTICANC R, 21(4B), 2001, pp. 3053-3059
Background: Different oncogenes (Fas and bcl-2) and diverse cytokines (IL-1
0 and alfa-TNF) may have an effect on the regulation of apoptosis. The majo
rity of studies to elate have evaluated only one or two of these elements i
ndependently and it is difficult to obtain a global view of apoptosis disre
gulation in the pathogenesis of systemic lupus erythematosus (SLE) and thei
r role in disease activity. The aim of this study was to evaluate serum lev
els of sFas, bcl-2, IL-10 and alfa-TNF in human SLE patients and to analyze
their relationship with disease activity and with regulation of the apopto
tic process. Patients and Methods: Serum levels of sFas and cytokines IL-10
and alfa-TNF were studied by enzyme-linked immunoabsorbent assay. Bcl-2 an
tigen expression was analyzed in lysated lymphocytes from 51 SLE patients.
The disease activity was analyzed according to the SLE disease activity ind
ex (SLEDAI). Results: SLE patients had higher levels of sFas (p = 0.0006) a
nd alfa-TNF (p < 0.0001) than the control group. No relationship was found
between the levels of bcl-2 and IL-10 from SLE patients and the control gro
up. However, there was a significant correlation between SLEDAI and bcl-2 (
p < 0.001) and IL-10 levels (p = 0.004). In contrast, we found that sFas an
d alfa-TNF were not related with disease activity. A significant correlatio
n of sFas with alfa-TNF serum levels (p = 0.003, R = +0.41) and bcl-2 antig
en expression (p = 0.02, R = +0.32) was observed. Conclusion: sFas and alfa
-TNF serum levels are increased in SLE patients. sFas levels seems to be se
condary to alfa-TNF action, which is enhanced in inflammatory conditions su
ch as SLE. Bcl-2 antigen expression and IL-10 serum levels are related to t
he maintenance of SLE activity. These alterations may interfere with the ap
optotic process, promoting lymphocyte hyperactivity secondary to increased
cytokine levels, and causing the characteristic features of SLE.